a diverse group of congenital brain abnormalities that arise specifically from defective formation of the central nervous system .
Due to the congenital nature of neuronal migration disorders, most patients do not recover from their symptoms. The course of disease tends to be static.
The most well characterized genes include DCX on the X chromosome, responsible for double cortex syndrome, and LIS1 on chromosome 17, the first gene identified for lissencephaly.
Diagnosis is usually made by neuroimaging. CT scan or MRI of the brain will show the characteristic abnormality. MRI has better resolution and may detect polymicrogyria or small heterotopias more easily than CT.
Maybe the lineage of giant cells has to do with neuronal migration.
In lissencephaly or agyria, neuronal migration fails globally, causing the brain to appear completely smooth and have abnormal layering in the cortex.
Lissencephaly is part of a spectrum of brain malformations, which are referred to as the agyriapachygyria-band spectrum and are caused by abnormalities in neuronal migration, a critical process in brain development
Neuronal acetylcholine receptor (AChR) ganglionic alpha-3 antibodies in the blood are often associated with autoimmune conditions, particularly those affecting the nervous system. Their presence may indicate disorders such as autoimmune autonomic neuropathy or Lambert-Eaton myasthenic syndrome. These antibodies can interfere with normal neuronal signaling, leading to symptoms related to autonomic dysfunction. Detection of these antibodies typically warrants further investigation and management by a healthcare professional.
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Clusters of neuronal cell bodies and dendrites in the brain are called nuclei.
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Neuronal dropout refers to the loss of neurons in the brain due to various factors such as aging, neurodegenerative diseases, or injury. This can lead to cognitive decline and impaired brain function. Strategies to promote neuroprotection and neurogenesis can help mitigate neuronal dropout.